The effects of cannabis consumption are dependent on many factors, including (3,4):

• The dose of cannabis consumed
• The ratio of the various cannabinoids in the cannabis product
• The route of administration
• The timing – the effects of cannabis are different right after consumption as compared to hours after consumption
• The health status of the patient
• The age of the patient - exposure of THC impacts the developing brain of a child or adolescent differently than the fully developed brain of an adult; adults are more resistant to cannabis-induced behavioral and brain morphological changes (5). Also, elderly patients may be more sensitive to many of the effects of cannabis.
• The co-administration of other drugs/medicines
• Whether or not the patient has been using cannabis recreationally (or receiving cannabis therapy) long-term or if the patient is cannabis naïve
• Setting within which the cannabis use takes place (e.g., some of the affective reactions – levity, anxiety, panic - may be shaped by the social environment and perceived comfort of the consumer)

Cannabis affects psychological function, cognitive and psychomotor function, sensory perception and motor function, as well as other neurological functions. The effects of cannabis use on neurologic function are reviewed below.

Psychological effects: A majority of the acute psychoactive effects of cannabis, including euphoria, relaxation, anxiety and/or paranoia are due to tetrahydrocannabinol's (THC) binding activity (3). When it binds to CB1 receptors in the CNS, THC stimulates the release of high amounts of dopamine, and this, in turn, leads to the onset of euphoria and relaxation (5). Cannabis consumption may also acutely induce anxiety attacks and psychotic symptoms, and does so more commonly in cannabis-naïve individuals and in individuals who have consumed high amounts of THC. In contrast to THC, CBD does not induce a ‘high' or anxiety, and CBD may actually attenuate THC's euphoric and psychoactive effects without altering THC's relaxing effect (6,7).

The duration and intensity of the adverse acute psychological effects may be greater after oral consumption as compared to inhalation. (This is due to the first pass metabolism of THC that occurs after oral consumption.) Of note, the monograph of nabilone (a synthetic form of THC taken orally) states that the adverse psychotropic reactions can persist for 48 to 72 hours following cessation of treatment (8). There are no medications approved specifically for the treatment of anxiety, panic and psychosis associated with cannabis intoxication, but benzodiazepines or second-generation (atypical) anti-psychotic medication have been suggested (9).

As for the psychological effects of the long-term use of cannabis and cannabinoids, the National Academy of Sciences' 2017 report states that:

• "There is substantial evidence of a statistical association between cannabis use and the development of schizophrenia or other psychoses, with the highest risk among the most frequent users" (2).
• "There is moderate evidence that, in individuals with schizophrenia and other psychoses, a history of cannabis use may be linked to better performance on learning and memory tasks" (2).
• "There is limited evidence of a statistical association between cannabis use and the development of any type of anxiety disorder, except social anxiety disorder. There is moderate evidence of a statistical association between regular cannabis use and increased incidence of social anxiety disorder" (2).
• "There is limited evidence of a statistical association between cannabis use and the likelihood of developing bipolar disorder, particularly among regular or daily users. And, for individuals diagnosed with bipolar disorders, near daily cannabis use may be linked to greater symptoms of bipolar disorder than non-users" (2).
• "There is moderate evidence of a statistical association between cannabis use and increased incidence of suicidal ideation and suicide attempts, with a higher incidence among heavier users" (2).
• "There is moderate evidence of a statistical association between cannabis use and increased symptoms of mania and hypomania in individuals diagnosed with bipolar disorders (regular cannabis use)" (2).
• "There is moderate evidence of a statistical association between cannabis use and a small increased risk for the development of depressive disorders" (2).

(For a detailed discussion on the association between cannabis use and psychiatric disorders, the reader is referred to the section entitled "Cannabis Use and Mental Health" in this cannabis curriculum.)

Sedative effects: Cannabis is a CNS depressant and may cause drowsiness or somnolence. Its CNS depressant effects are additive with other CNS depressants, including opioids (3). There is moderate evidence that cannabis or cannabinoids are effective for improving short-term sleep outcomes in individuals with sleep disturbance associated with obstructive sleep apnea syndrome, fibromyalgia, chronic pain, and multiple sclerosis (2).

Cognitive and psychomotor function (acute and long-term) effects: There is moderate evidence of a statistical association between acute cannabis use and the impairment in the cognitive domains of learning, memory and attention (2). Reasoning and the ability to perform tasks requiring complex motor skills may become impaired, and thoughts may become non-cohesive after cannabis consumption (3,4). The ingestion of cannabinoid medications such as dronabinol and nabilone (synthetic versions of delta -9-THC for oral consumption), and nabiximols (Sativex, an oromucosal spray) has been associated with decreased psychomotor performance. In the drug monographs of these cannabinoid products, patients are warned not to drive or operate complex machinery after consuming the medication (8,10,11).

Long-term (recreational) use of cannabis during adolescence is related to impairments in subsequent academic achievement and education, and employment. (2,5). And, a limited number of studies suggest that there are impairments in cognitive domains of learning, memory and attention, even in individuals who have stopped smoking cannabis (2). According to a cross sectional study by Honarmand et al., prolonged use of ingested or inhaled cannabis in multiple sclerosis patients was associated with a poorer performance in multiple cognitive areas, including working memory, executive functions and speed of information processing (12). Interestingly, in a prospective cohort study describing safety issues among medical cannabis patients with non-cancer chronic pain, neurocognitive function improved in the medical cannabis group (13).

Motor function effects: Initially, the inhalation of cannabis may cause an increase in motor activity, but this increase in activity is often followed by a decrease in overall motor activity. Coordination is negatively impacted, and ataxia, dysarthria and general weakness are not uncommon (3). According to the drug monographs of nabilone and dronabinol, some individuals who have taken these synthetic THC oral medicines have experienced tremors, ataxia, and rarely seizures (8,10).

Of note, there is limited evidence that cannabis or cannabinoids are effective for improving symptoms of Tourette syndrome (2) and other movement disorders (4). However, studies have suggested that cannabinoids effectively reduce the spasticity associated with multiple sclerosis, and the American Academy of Neurology proposes that the use of oral cannabinoid extracts or an oromucosal cannabinoid spray (1:1 THC:CBD) by MS patients may reduce symptoms of spasticity (14).

Perception and sensory effects: Some of the acute effects of cannabis consumption include hallucinations, visual-spatial perception distortion, blurred vision, changes in perceived brightness, and time distortion, (5,7). Individuals may also experience an increased intensity of tactile, auditory and taste sensations (1, 2). Complex perceptual alterations may include a sense of detachment from aspects of one's own body (depersonalization) or a feeling that one's environment has undergone some inexplicable change (derealization).

Whether inhaled or consumed orally or oromucosally, cannabis has been reported to have analgesic properties similar to that of codeine's analgesic effects (3), but its mechanism of action is different. Results of a year-long prospective cohort study with 215 study patients and 216 controls, showed significant improvements in pain intensity among the medical cannabis users compared with controls (13).

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

You must purchase the New York State Practitioner Education - Medical Use of Marijuana Course to view - click here to Purchase Course Credit.

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Author(s):

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References:

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